1. Field of the Invention
The present invention generally relates to a method and composition for the alleviation of eye diseases and, more specifically, to an improved method and composition for combating macular degeneration.
2. Description of the Related Art
Macular degeneration associated with aging and drusen is an extremely significant concern, and is now a major cause of blindness in the United States for individuals over 65 years of age. Just at the period of time when the eyes are a most important sense, and reading and watching television are often the most enjoyable avenues of entertainment, this disease robs the elderly patient of such possibilities.
The crystalline lens of the eye has only one disease state that we are aware of, and that is cataract. The lens loses its clarity as it becomes opacified, and vision is disturbed depending on the degree of opacification. There are different etiologies for cataracts such as a congenital lesion or trauma, which are well recognized. It is also known that some medicines such as cortisone-type preparations and glaucoma medications can cause cataracts, as can inborn metabolic errors such as galactosemia. These, however, are relatively uncommon in comparison to the common aging cataract, which shows an increase in frequency directly correlated with age.
The exact incidence of cataracts in the general population is difficult to determine because it depends on one's definition of a cataract. If defined as simply a lens opacity, then obviously the incidence is much higher than when defined as a lens opacity that significantly impacts vision. The pathogenesis of age-related cataracts and macular degeneration is incompletely understood.
Macular degeneration associated with aging and drusen also appears to be a biodegeneration with no effective treatment to date except with laser treatment in patients who develop abnormal vessels under the retina, i.e., subretinal neovascularization. The treatable group is a distinct minority of a much larger group. That means that individuals so afflicted can anticipate either a progressive deterioration or at times relatively static course, but no spontaneous improvement, since the basic architecture of the retina is destroyed. Occasionally, there may be variations in vision which seem to show improvement depending on such things as lighting in the room and potential resolution of fluid underneath the retina. The important point, however, is that when this sensitive neurologic tissue is damaged, that damage is permanent.
In 1981, Spector et al. stated that there still remained questions concerning the mechanism and agents involved with massive oxidation of the lens tissue and its relationship to cataract development. Spector, Exp. Eye Res., 33:673, 1981. They also noted that glutathione (GSH) can act as a reducing agent and free radical trapper. GSHPx and catalase are present to metabolize H.sub.2 O.sub.2. SOD can detoxify O.sub.2, and light can photochemically induce oxidation. However, Spector et al. believed that the actual roles of light and/or metabolically-generated oxidized components are unclear as to causing the observed oxidation products.
In 1987, Machlin et al. reported that there was some evidence that free radical damage contributed to the etiology of some diseases, including cataract. FASEB J. 1:441-45, 1987. They indicated that defenses against such free radical damage included Vitamin E, Vitamin C, betacarotene, zinc, iron, copper, manganese, and selenium.
As recently as 1988, in an article by Jacques et al., "Antioxidant Status in Persons With and Without Senile Cataract," Arch. Ophthal. 106:337, 1988, it is reiterated that it is commonly believed that oxidative mechanisms are causally linked to, not simply associated with, cataract formation. According to Jacques et al., the evidence suggests that GSHPx and SOD decrease with increasing degree of cataract.
Jacques et al. further reported that Vitamin E is believed to be a determinant of cataract formation and can act synergistically with GSHPx to prevent oxidative damage. They point out the possibility that Vitamin C may have a role in cataract formation and might influence GSHPx through its ability to regenerate Vitamin E.
If a treatment modality could slow down the progression of cataracts or macular degeneration, it would have a tremendous impact on the number of individuals who suffer from these problems due to the fact that they both occur toward the end of life. Toxicity from free radicals and oxidizers has generated significant interest in both diseases. There is circumstantial evidence at present to indicate that protection against phototoxicity and oxidizers could slow the onset and progression of both ailments.
While the problems associated with cataracts and macular degeneration have long been recognized, and many attempts have been made to identify the causative factors and to solve such problems, those diseases still remain as major health problems.
A need therefore still exists in the art to provide improved methods and compositions for the treatment of macular degeneration in the absence of a surgical solution.